Endothelial Progenitor Cells, Endothelial Dysfunction, Inflammation, and Oxidative Stress in Hypertension

内皮功能障碍 高血压的病理生理学 氧化应激 炎症 内皮 平衡 医学 一氧化氮 病理生理学 血管收缩 血管舒张 内科学 内分泌学 生物信息学 免疫学 生物 血压
作者
Timothy Watson,Patrick K. Y. Goon,Gregory Y.H. Lip
出处
期刊:Antioxidants & Redox Signaling [Mary Ann Liebert]
卷期号:10 (6): 1079-1088 被引量:102
标识
DOI:10.1089/ars.2007.1998
摘要

With a prevalence in excess of 20%, hypertension is a common finding among Western adult populations. Hypertension is directly implicated in the pathophysiology of various cardiovascular disease states and is a significant contributor to ill health, leading to an excess of both morbidity and mortality. The etiology of hypertension has been explored in depth, but the pathophysiology is multifactorial, complex, and poorly understood. Recent interest has been directed toward investigating the purported role of the endothelium, which acts as an important regulator of vascular homeostasis. Endothelial dysfunction is now recognized to occur in hypertension, regardless of whether the etiology is essential or secondary to endocrine or renal processes. Nitric oxide (NO) is a volatile gas produced by endothelial cells that acts to maintain vascular tone. Reduced bioavailability of NO appears to be the key process through which endothelial dysfunction is manifested in hypertension. The result is of an imbalance of counteracting mechanisms, normally designed to maintain vascular homeostasis, leading to vasoconstriction and impaired vascular function. It has become increasingly apparent that these changes may be effected in response to enhanced oxidative stress, possibly as a result of systemic and localized inflammatory responses. This article provides an overview of endothelial dysfunction in hypertension and focuses on the purported role of oxidative stress and inflammation as the catalysts for this process.
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